OXYGEN-UPTAKE AND LUNG-FUNCTION IN MICE INFECTED WITH STREPTOCOCCUS-PNEUMONIAE, INFLUENZA-VIRUS, OR MYCOPLASMA-PULMONIS

Abstract

Model systems of respiratory infection in mice were established with S. pneumoniae, influenza virus and M. pulmonis. The LT50 [50% mortality] for S. pneumoniae was 2 1/2 days, for lethal influenza 6 days and for M. pulmonis 5 days. Morbidity in sublethal influenza infections reached a peak during days 5-10, with recovery indicated by the 3rd week. The course of each pulmonary infection was followed by use of the animal''s maximal ability to consume oxygen (.ovrhdot.VO2 max), by determining the weight, compliance and stability of the excised lung, and in some cases by following O2 consumption of minced tissue. Depression of .ovrhdot.VO2 max began early in each infection; reductions ranged from 9% at the peak of sublethal influenza infection to 50% 12-48 h before the LT50 of fatal infections. The depressions were not relieved by 100% O2. The noninvasive .ovrhdot.VO2 max test, evoked by cold air, was simple, rapid and reproducible and appeared to serve as a quantitative measure of over-all function during infection. Each type of infection caused an increase in lung weight, with the largest noted during fatal Mycoplasma illness and lethal influenza. The effects on lungs by influenza and M. pulmonis infections were similiar but could be differentiated from those with S. pneumoniae. With sublethal influenza, CL [lung complicance] was reduced 30% between days 5-10, with recovery by the 3rd week. Ctis [tissue complicance] was not affected. M. pulmonis infections and lethal influenza caused depressions in CL of over 60% by day 4 but only a 30% decrease in Ctis. The decreased compliance in influenza and M. pulmonis infections was apparently due primarily to increased surface tension. S. pneumoniae did not affect complicance.